Bottom Line:
Here, we investigated whether neural responses to others' pain vary with psychopathic traits within the general population in a similar manner to that found in individuals at the extreme end of the continuum.As predicted, variation in psychopathic traits was associated with variation in neural responses to others' pain in the network of brain regions typically engaged during empathic processing.That is, after controlling for the influence of the other dimension, higher affective-interpersonal psychopathic traits were associated with reduced neural responses to others' pain, whilst higher lifestyle-antisocial psychopathic traits were associated with increased neural responses to others' pain.

ABSTRACTDisrupted empathic processing is a core feature of psychopathy. Neuroimaging data have suggested that individuals with high levels of psychopathic traits show atypical responses to others' pain in a network of brain regions typically recruited during empathic processing (anterior insula, inferior frontal gyrus, and mid- and anterior cingulate cortex). Here, we investigated whether neural responses to others' pain vary with psychopathic traits within the general population in a similar manner to that found in individuals at the extreme end of the continuum. As predicted, variation in psychopathic traits was associated with variation in neural responses to others' pain in the network of brain regions typically engaged during empathic processing. Consistent with previous research, our findings indicated the presence of suppressor effects in the association of levels of the affective-interpersonal and lifestyle-antisocial dimensions of psychopathy with neural responses to others' pain. That is, after controlling for the influence of the other dimension, higher affective-interpersonal psychopathic traits were associated with reduced neural responses to others' pain, whilst higher lifestyle-antisocial psychopathic traits were associated with increased neural responses to others' pain. Our findings provide further evidence that atypical function in this network might represent neural markers of disrupted emotional and empathic processing; that the two dimensions of psychopathy might tap into distinct underlying vulnerabilities; and, most importantly, that the relationships observed at the extreme end of the psychopathy spectrum apply to the nonclinical distribution of these traits, providing further evidence for continuities in the mechanisms underlying psychopathic traits across the general population.

Fig1: Partial regression plots showing opposing relationships between response to pain > no-pain in bilateral anterior insula (AI), inferior frontal gyrus (IFG), and midcingulate cortex (midCC), as well as unique variances associated with affective-interpersonal and lifestyle-antisocial psychopathic traits after the other dimension had been controlled for (a similar pattern was also seen in the anterior cingulate cortex [ACC], adjacent to midCC). (Left) Negative relationships between blood oxygenation-level-dependent (BOLD) response to pain > no-pain and affective-interpersonal traits after controlling for the effect of lifestyle-antisocial traits. (Right) Positive relationships between BOLD response to pain > no-pain and lifestyle-antisocial traits after controlling for the effect of affective-interpersonal traits. R2 reflects the partial correlation coefficients of determination. The insets show horizontal and midsagittal sections of the bilateral AI (z = 0), IFG (z = 15), and midCC (x = 0) regions of interest, overlaid on an average T1 structural image from all participants

Mentions:
Whole-brain analyses for the pain > no-pain contrast are reported using a cluster-forming threshold of p < .001 (uncorrected, cluster size > 10), with cluster-level family-wise error (FWE) correction. Region-of-interest (ROI) analyses were conducted in four a priori ROIs (bilateral AI, IFG, ACC, and midCC). The first three were taken from Lockwood et al. (2013), and the midCC was added because it regularly features in meta-analyses of empathy for pain, with clusters bordering midCC and ACC (Fan et al., 2011; Lamm et al., 2011). ROI analyses were conducted as described by Lockwood et al. ROIs were anatomically defined using masks from the automated anatomical labeling atlas (Maldjian, Laurienti, Kraft, & Burdette, 2003), and the MarsBaR toolbox (http://marsbar.sourceforge.net) was used to calculate average contrast estimates across bilateral ROIs and to conduct t tests at a standard statistical threshold of p < .05 (Eisenberger et al., 2010; Masten et al., 2011). The contrast estimates extracted with MarsBaR were also used in IBM SPSS and MS Excel to conduct regression analyses and to generate the illustrative partial regression plots presented in Fig. 1 below.Fig. 1

Fig1: Partial regression plots showing opposing relationships between response to pain > no-pain in bilateral anterior insula (AI), inferior frontal gyrus (IFG), and midcingulate cortex (midCC), as well as unique variances associated with affective-interpersonal and lifestyle-antisocial psychopathic traits after the other dimension had been controlled for (a similar pattern was also seen in the anterior cingulate cortex [ACC], adjacent to midCC). (Left) Negative relationships between blood oxygenation-level-dependent (BOLD) response to pain > no-pain and affective-interpersonal traits after controlling for the effect of lifestyle-antisocial traits. (Right) Positive relationships between BOLD response to pain > no-pain and lifestyle-antisocial traits after controlling for the effect of affective-interpersonal traits. R2 reflects the partial correlation coefficients of determination. The insets show horizontal and midsagittal sections of the bilateral AI (z = 0), IFG (z = 15), and midCC (x = 0) regions of interest, overlaid on an average T1 structural image from all participants

Mentions:
Whole-brain analyses for the pain > no-pain contrast are reported using a cluster-forming threshold of p < .001 (uncorrected, cluster size > 10), with cluster-level family-wise error (FWE) correction. Region-of-interest (ROI) analyses were conducted in four a priori ROIs (bilateral AI, IFG, ACC, and midCC). The first three were taken from Lockwood et al. (2013), and the midCC was added because it regularly features in meta-analyses of empathy for pain, with clusters bordering midCC and ACC (Fan et al., 2011; Lamm et al., 2011). ROI analyses were conducted as described by Lockwood et al. ROIs were anatomically defined using masks from the automated anatomical labeling atlas (Maldjian, Laurienti, Kraft, & Burdette, 2003), and the MarsBaR toolbox (http://marsbar.sourceforge.net) was used to calculate average contrast estimates across bilateral ROIs and to conduct t tests at a standard statistical threshold of p < .05 (Eisenberger et al., 2010; Masten et al., 2011). The contrast estimates extracted with MarsBaR were also used in IBM SPSS and MS Excel to conduct regression analyses and to generate the illustrative partial regression plots presented in Fig. 1 below.Fig. 1

Bottom Line:
Here, we investigated whether neural responses to others' pain vary with psychopathic traits within the general population in a similar manner to that found in individuals at the extreme end of the continuum.As predicted, variation in psychopathic traits was associated with variation in neural responses to others' pain in the network of brain regions typically engaged during empathic processing.That is, after controlling for the influence of the other dimension, higher affective-interpersonal psychopathic traits were associated with reduced neural responses to others' pain, whilst higher lifestyle-antisocial psychopathic traits were associated with increased neural responses to others' pain.

ABSTRACTDisrupted empathic processing is a core feature of psychopathy. Neuroimaging data have suggested that individuals with high levels of psychopathic traits show atypical responses to others' pain in a network of brain regions typically recruited during empathic processing (anterior insula, inferior frontal gyrus, and mid- and anterior cingulate cortex). Here, we investigated whether neural responses to others' pain vary with psychopathic traits within the general population in a similar manner to that found in individuals at the extreme end of the continuum. As predicted, variation in psychopathic traits was associated with variation in neural responses to others' pain in the network of brain regions typically engaged during empathic processing. Consistent with previous research, our findings indicated the presence of suppressor effects in the association of levels of the affective-interpersonal and lifestyle-antisocial dimensions of psychopathy with neural responses to others' pain. That is, after controlling for the influence of the other dimension, higher affective-interpersonal psychopathic traits were associated with reduced neural responses to others' pain, whilst higher lifestyle-antisocial psychopathic traits were associated with increased neural responses to others' pain. Our findings provide further evidence that atypical function in this network might represent neural markers of disrupted emotional and empathic processing; that the two dimensions of psychopathy might tap into distinct underlying vulnerabilities; and, most importantly, that the relationships observed at the extreme end of the psychopathy spectrum apply to the nonclinical distribution of these traits, providing further evidence for continuities in the mechanisms underlying psychopathic traits across the general population.